Liver disease Flashcards
acute hepatitis duration and etiology
b. ACUTE: <6 mo; self limited
i. Etiology: viruses, drugs, alcohol
chronic liver disease duration
c. CHRONIC: >6 mo; unresolving; often leads to cirrhosis
systemic infection whose primary manifestations are hepatic
viral infection
b. Serotypes: A, B, C, E, G
infection with the delta particle is dependent on concomitant infection with …
i. D (Delta) subtype of hepatitis B
what type of hepatitis is usually mild but severe in pregnancy
hepatitis E
seen with a 20% mortality in pregnancy
which type of hepatitis is associated with travel
Hep A
which hepatitis infections are usually more severe
B and C
more severe, higher incidence of morbidity & mortality
sxs associated with hepatitis infection (initial)
” Flu-like syndrome (fatigue, nausea, myalgias)
“ Abdominal Pain
70% of pts will be seen with these symptoms
70%
“ Tender, palpable liver
“ Posterior cervical LAD
“ Splenomegaly
“ Jaundice usually disappears 2-8 weeks after onset
**Have to get a pretty high bilirubin to get icterus
Labs that will help dx hepatitia
Transient anemia,
lymphocytosis with atypical lymphs,
increased reticulocyte count
reticulocytes
what are they and how do they relate to hepatitis
increased in hepatitis
= cells that come out of the bone marrow which will differentiate into WBC and RBC
- Bone marrow’s response is to make a bunch more of new cells in response to the transient anemia
Level of____ indicates severity of disease
ii. Increased direct and total serum bilirubin
1. Level indicates severity of disease; indicates level of jaundice
what increases in liver enzymes would you expect to see in a pt with hepatitis
- ALT typically higher than AST
2. Provides a rough estimate of hepatocellular injury but no prognostic value
when would we expect to see an elevated alk phos in a pt with hepatitis
iv. Alk Phos rises early ands often remains elevated after clinical recovery
what Prothrombin time would we expect to see in a pt wiht hepatitis
usually normal; if elevated suspect fulminant hepatitis
so much inflammation and destruction of liver that the liver is starting to fail
- Fulminant hepatitis
what is going on in Fulminant hepatitis
a. Liver is not making clotting factors anymore
b. This is a sign that pt is not going to do very well
Rapid fall in serum aminotransferase associated with
aminotransferase from high to normal in < 1 week may be an indication of fulminant hepatitis with massive necrosis / destruction of liver parenchyma
should not see significant drops
i. Acute viral hepatitis usually resolves completely in
1-3 weeks
how do you treat acute viral hepatitis
ii. Treat nausea, vomiting, anorexia
1. Compazine or other antiemetics
iii. Benadryl, Atarax
Benadryl, Atarax
- Sedatives may precipitate hepatic encephalopathy
- For their itching (sedating antihistamines)
- When bilirubin gets really high, their skin becomes really itchy. Pt’s w/ jaundice itch a lot
what should be avoided in acute hepatitis
iv. Avoid ETOH and tobacco use, hepatic cleared meds until 1 month after all labs return to normal
i. Most common type of acute hepatitis
a. Hepatitis A
characteristics commonly associated with hepatitis A epidemics
- Poor hygienic conditions
- Contaminated water supply
- Infected food handlers
- Ingestion of contaminated shellfish
- Institutions/daycare
iii. Doesn’t cause chronic hepatitis
high prevalence of Hep A in this country
Mexico
when did we start vaccinating children for hepatitis A
what is the dosing?
- Incorporated into routine childhood vaccination schedule in 2006
a. 2 doses starting at 12 mos, 6-12 mos apart
when would you vaccinate an adult for hepatitis A
- recommended for high risk individuals
a. Chronic liver disease
b. Clotting disorders - should be vaccinated against A and B
c. Occupational or travel exposure
gold standard for dx hepatitis A
” Serum anti-HAV IgM antibodies gold standard detecting acute illness
when would you expect to see positive Anti-HAV antibodies in a pt with heptatis A
” Anti-HAV positive at onset of sx, peaks during convalescent phase, remains positive 4-6 mos
other than anti-HAV IgM what other labs would we expect to see
” Serum ALT > AST (b/c viral)
“ Bilirubin > 10 common
Hep A does have positive antibodies test at ONSET of symptoms
Tx for hepatitis A
tx is supportive
acute infection confers immunity
prognosis
- 85% have full recovery w/in 3 months and nearly all have complete recovery by 6 months
Fatalities most common in elderly or those with chronic Hep C or with other comorbidities
ULN for ALT
iii. Upper limit of normal is around 40 for ALT
ULN for alk phos
iv. 150 = upper normal limit for Alk Phos
v. 1= upper normal limit for Tbili
transmission fo hep b
i. Usual transmission is blood borne
- IV drug use or vertical transmission from mom to baby most common
ii. Less common: sexual transmission
A 56 yo male calls your office c/o 1 week h/o fatigue, flu-like symptoms, abdominal pain and nausea. He has been using “those contaminated berries from Costco” in health shakes for the past 6 weeks. On PE he appears WDWN, fatigued but in NAD; VSS; no icterus or jaundice, liver tender without HSM, neg Murphy’s sign, no peritoneal signs
what labs would you get
- CBC normal
- Elevated LFT’s: ALT 300, AST 200, Alk Phos 250, Tbili 2.5
- Anti-HAV IgM positive
hep a
supportive care
A 56 yo male calls your office c/o 1 week h/o fatigue, flu-like symptoms, abdominal pain and nausea. He has been using “those contaminated berries from Costco” in health shakes for the past 6 weeks. On PE he appears WDWN, fatigued but in NAD; VSS; no icterus or jaundice, liver tender without HSM, neg Murphy’s sign, no peritoneal signs
what would be the follow up for this pt
- Recheck his LFTs within a week, if symptoms get worse then come in sooner and recheck sooner - repeat CBC and LFTs
a. Don’t need to recheck hepatic antibody
what other hepatitis is associated with Hep B
iii. Delta agent (Hep D): defective virus particle, same route of transmission assoc with Hep B
- Causes clinical exacerbation for Hep B carriers
- Implicated in fulminant hepatitis
- Rapid progression to cirrhosis
who do we give the hep B vaccine to?
- Recommended for everyone
a. Given at birth
b.
3 doses at 0, 2, 6 months (varying schedules)
c. Post-exposure prophylaxis
d. High risk individuals
i. Health care workers, sex workers
how do we diagnose hep b
” HBsAg present 1-10 wks after acute exposure
“ Usually undetectable after 6 months
“ Persistence of HBsAg after 6 months implies chronic infection/carrier state
how frequently do we see chronic hep b infections
< 1% of immunocompetent pts will progress to chronic infection
what ALT AST would we expect to see in a pt with hep B
- ALT & AST elevated up to 2000 in acute phase with ALT higher than AST
best predictor of prognosis in a pt with Hep B
- PTT or PT/INR is the best predictor of prognosis
what does a PTT tell us about the status of a Hep B infection
a. Elevation of INR = they are starting to bleed more AKA liver is not functioning well/not making clotting factors
what ALT would indicate chronic hep B infection
normalization of LFT’s in 1-4 months
4. Persistent elevation of ALT > 6 months = progression to chronic hepatitis
Hep B treatment goal
o Goal: suppression of viral replication
Hep B indications for Tx (5)
o Indications for treatment
- acute liver failure
- clinical complications of cirrhosis
- advanced fibrosis with high serum HBV DNA, or reactivation of chronic HBV after chemotherapy or immunosuppression.
- INR >1.5
- fulminant hepatitis
incidence of chronic Hep b infection by age
- 90% perinatal
- 20-50% for age 1-5 years
- < 5% for adults
sxs of a chronic hep b infection
: nonspecific; fatigue; acute exacerbations of infection that mimic acute hepatitis; hepatic failure
a. HBeAg is a marker for
HBV replication and degree of infectivity
Patients in low or nonreplicating phase / inactive carrier state are HBeAg negative
b. Low infectivity b/c low amounts of virus is replicating
when would you have a carrier of hep b with risk of infectivity
- Persistent Positive HBsAg > 6 mo following acute infection
iv. Evaluation of pts w/ chronic HBV infection
a. Hx and PE
b. Fam hx of liver dz, HCC
c. Lab tests
d. Tests for HBV replication
e. Tests to r/o viral coinfection
f. Tests to screen for HCC
what lab tests would you want for a pt suspected of chronic hep b
CBC w/ platelets, hepatic panel, prothrombin time
what tests for HBV replications would you want for a pt suspected of i
HbeAg/anti-HBe, HBV DNA
what Tests to screen for HCC would you run in a pt with hep b
AFP at baseline and in high risk pts US as well
- Suggested f/up for chronic hep b pt
a. Screen w/ surface antigen. Confirm w/ hep panel and envelope panel, get an INR, get an AFP level, possibly an US as well. Refer to GI to see if they need liver biopsy
- 5 year prognosis for progression to cirrohsis in a pt with hep b
a. Cirrhosis 12 - 20%
.5 year prognosis for hep b progression to Hepatic failure 20%
Hepatic failure 20%
5 year prognosis for hep b progression to Hepatocellular Carcinoma
c. Hepatocellular Carcinoma 15%
Lifetime mortality from liver disease in pt with chronic hep b
= 50%
what is the incidence of eradication and reactivation associated with chronic hep b
- Complete eradication rarely occurs after acute infection
4. Immunocompromised pts more likely to have reactivation, progression
i. Most common chronic liver disease
Hep c
, accounts for 8,000 to 13,000 deaths each year
ii. Majority of liver transplants in the US
what does acute hep c look like and how many progress
Up to 80% progress to chronic infection leading to fibrosis and cirrhosis
what % of hep c develops into cancer
- 3% of these develop hepatocellular CA
2. Accounts for 30% of HCC cases in US
HCV screening guidelines
- Anyone born in the United States between 1945 and 1965
- Those with h/o illicit IVDU or intranasal cocaine use, even if only used once
- Those who received clotting factors made before 1987
- Those who received blood/organs before July 1992
- Those who have been informed that they received blood from a donor who later tested positive for HCV
- Those who were ever on chronic hemodialysis
- Those with evidence of liver disease (persistently elevated ALT level)
- Those infected with HIV
- Children born to HCV-infected mothers
- Those with a needle stick injury or mucosal exposure to HCV-positive blood
- Those who are a current sexual partner of an HCV-infected person
what is most commonly used to dx HCV
” Anti HCV ELISA allows detection in about 95% of pts 2 weeks after exposure
most sensitive test for hep c
HCV RNA by PCR
if you have a positive anti HCV but negative HCV RNA
you have resolution or acute HCV
if you have negative anti HCV and positive HCV RBA
early acute HCV or chronic HCV in the setting of an immunosuppressed person
besides HCV RNA and antibody testing how else should you evaluate HCV
- Determination of HCV genotype is essential to making decisions about treatment
- Assessment for liver fibrosis through biopsy or noninvasive measures is helpful in guiding decisions regarding treatment and surveillance
- Testing for HIV, hepatitis B, and hepatitis A
a. Vaccination should be administered to those without immunity to Hep A & B
how many different genotypes of HCV are there and what kind is prevalant in the US
- 6 different genotypes of Hep C
- United States - genotype 1 MC
a. Can essentially cure Hep C in the US - Africa í genotype 4 is MC which is more difficult to treat
mngmt of hep c
- Antiviral therapy
- Psychologic counseling
- Alcohol avoidance
- Symptom control
- Dose adjustment of medications
- Assessment of fibrosis
- Screening for complications of cirrhosis if present
HCV treatment
- The goal of treatment in patients with chronic HCV is to eradicate HCV RNA, which is associated with decreases in all-cause mortality, liver-related death, need for liver transplantation, hepatocellular carcinoma rates, and liver-related complications
- All patients with detectable viral load >6 mos should consider treatment
- Treatment selection varies by genotype and other patient factors
- Cirrhosis
: late stage of progressive hepatic fibrosis; distortion of the hepatic architecture and the formation of regenerative nodules
what is the mngmt of cirrhosis
- Generally irreversible in advanced stages
- In earlier stages, specific treatments aimed at the underlying cause of liver disease may improve or even reverse cirrhosis
- W/ cirrhosis - Harvoni for 12 weeks = 1st line therapy
when would you want to recheck viral loads after recovery
- Recheck viral loads at 12 & 24 wks
what is the definition of recovery from HCV
SVR = sustained viral response
SVR defined as undetectable viral load after 24 wks
prognosis of hep c
Survival linked to development of cirrhosis
Cirrhosis in about 50% of pts with chronic Hep C
Cirrhosis = 3% per year chance developing HCC
Widespread hepatic fibrosis
Cirrhosis
onset and sxs associated with cirrhosis
iii. Insidious onset with nonspecific sxs
fatigue, anorexia, weight loss, nausea, abdominal pain
LABS for cirrhosis
- Anemia, Thrombocytopenia
- Elevated bilirubin, Decreased albumin
- Increased bleeding time
- Elevated ammonia associated with hepatic encephalopathy
a. Get confusion,
what are the signs of hepatic encephalopathy and what are the signs and medications that increase incidence
benzos and antihistamines both increase risk of encephalopathy because they are CNS medications
Get confusion, asterixis (shaking hands from hepatic encephalopathy)
management of cirrhosis
does need to be managed by a specialist
- Diuretics to help w/ fluid overload
- Paracentesis when they develop the ascites
- Vitamin K - once their INR increases, can give Vit K injections to control their coagulopathy
- Multivitamins
- Lactulose (reduces ammonia level)
- Avoid ETOH
- Liver transplant
complications of cirrhosis (5)
- Hepatic encephalopathy
- Bleeding from varices - very common
a. Varicose veins in their esophagus and portal hypertension in their belly. B/c of increasing bleeding time the varices will bleed - Ascites
- Spontaneous bacterial peritonitis
- Hepatocellular CA
why would a pt with cirrhosis develop pancreatitis
due to the development of cirrhosis
why would you see spontaneous bacterial peritonitis in a pt with cirrhosis
w/ ascites they get bacterial infection in their peritoneal fluid
a. Need to be treated with broad spectrum abx
what type of hepatitis would you be least likely to see a pt with the development of fulminant hepatitis
A
when do you see the onset of fulminant hepatitis
e. Onset within 8 weeks of disease
f. High mortality
what is the treatment of fulminant hepatitis
liver transplant
serological markers for hepatitis
o Hep A: Surface antigen/ antibody
- Acute infection confirmed by + IgM Anti HAV
o Hep B: surface antigen/ core antibody
- Acute infection confirmed by + HBsAg or Anti-HBc;
- delta agent: Anti HDV
- Anti-HBs= long term immunity to Hep B infection
o Hep C: HCV RNA by PCR
o Hep E : HEV RNA by PCR
Drug that is commonly associated with hepatitis
INH (tb)
also
“ Anabolic steroids
“ IV tetracycline
“ Acetaminophen overdose
biggest clue to alcoholic hepatitis
AST will be greater than ALT
how many alcoholic induced hepatitis progress to cirrhosis
g. 33% progress to cirrhosis
h. Risk of hepatic encephalopathy
when do we see alcoholic hepatitis
what are the symptoms
a. Occurs after prolonged (10 yrs) heavy intake
b. Anorexia, fatigue, jaundice
c. Tender hepatosplenomegaly
d. Fever, leukocytosis
Hx
i. Fever, RUQ pain, pruritus, skin rash, eosinophilia, increased transaminases
